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The pGEM-T is 3kb in length, and contains the amplicin resistance gene, conferring selection of the plasmid in E. coli, and the ori site which is the bacterial origin of replication. The plasmid has multiple cloning sites as shown below. The coding sequence was inserted by TA cloning. Many E. coli strains are suitable for the propagation of this vector including JM109, DH5α and TOP10.
The coding sequence can be easily obtained by digesting the vector with proper restriction enzyme(s). The coding sequence can also be amplified by PCR with M13 primers, or primer pair SP6 and T7.
|Mouse IL9 ORF mammalian expression plasmid, C-GFPSpark tag||MG51302-ACG|
|Mouse IL9 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||MG51302-ACR|
|Mouse IL9 ORF mammalian expression plasmid, C-Flag tag||MG51302-CF|
|Mouse IL9 ORF mammalian expression plasmid, C-His tag||MG51302-CH|
|Mouse IL9 ORF mammalian expression plasmid, C-Myc tag||MG51302-CM|
|Mouse IL9 ORF mammalian expression plasmid, C-HA tag||MG51302-CY|
|Mouse IL9 Gene cDNA clone plasmid||MG51302-G|
|Mouse IL9 ORF mammalian expression plasmid, N-Flag tag||MG51302-NF|
|Mouse IL9 ORF mammalian expression plasmid, N-His tag||MG51302-NH|
|Mouse IL9 ORF mammalian expression plasmid, N-Myc tag||MG51302-NM|
|Mouse IL9 ORF mammalian expression plasmid, N-HA tag||MG51302-NY|
|Mouse IL9 natural ORF mammalian expression plasmid||MG51302-UT|
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Interleukin 9, also known as IL-9, is a cytokine (cell signalling molecule) belonging to the group of interleukins. IL-9 is a cytokine that acts as a regulator of a variety of hematopoietic cells. This cytokine stimulates cell proliferation and prevents apoptosis. It functions through the interleukin 9 receptor (IL-9R), which activates different signal transducer and activator (STAT) proteins and thus connects this cytokine to various biological processes. Genetic studies on a mouse model of asthma demonstrated that this cytokine is a determining factor in the pathogenesis of bronchial hyperresponsiveness. IL-9 is a key molecule that affects differentiation of TH17 cells and Treg function. IL-9 predominantly produced by TH17 cells, synergizes with TGF-β1 to differentiate naïve CD4+ T cells into TH17 cells, while IL-9 secretion by TH17 cells is regulated by IL-23. Interestingly, IL-9 enhances the suppressive functions of FoxP3+ CD4+ Treg cells in vitro, and absence of IL-9 signaling weakens the suppressive activity of nTregs in vivo, leading to an increase in effector cells and worsening of experimental autoimmune encephalomyelitis. The mechanism of IL-9 effects on TH17 and Tregs is through activation of STAT3 and STAT5 signaling. Our findings highlight a role of IL-9 as a regulator of pathogenic versus protective mechanisms of immune responses.